clinical presentation of food induced anaphylaxis

MATTHEW C. PFLIPSEN, MD, AND KARLA M. VEGA COLON, MD

Am Fam Physician. 2020;102(6):355-362

Author disclosure: No relevant financial affiliations.

Anaphylaxis is a life-threatening systemic reaction, normally occurring within one to two hours of exposure to an allergen. The incidence of anaphylaxis in the United States is 2.1 per 1,000 person-years. Most anaphylactic reactions occur outside the hospital setting. Urticaria, difficulty breathing, and mucosal swelling are the most common symptoms of anaphylaxis. The most common triggers are medications, stinging insect venoms, and foods; however, unidentified triggers occur in up to one-fifth of cases. Coexisting asthma, mast cell disorders, older age, underlying cardiovascular disease, peanut and tree nut allergy, and drug-induced reactions are associated with severe or fatal anaphylactic reactions. Clinicians can obtain serum tryptase levels, reflecting mast cell degranulation, when the clinical diagnosis of anaphylaxis is not clear. Acute management of anaphylaxis involves removal of the trigger; early administration of intramuscular epinephrine; supportive care for the patient's airway, breathing, and circulation; and a period of observation for potential biphasic reactions. Only after epinephrine administration should adjunct medications be considered; these include histamine H 1 and H 2 antagonists, corticosteroids, beta 2 agonists, and glucagon. Patients should be monitored for a biphasic reaction (i.e., recurrence of anaphylaxis without reexposure to the allergen) for four to 12 hours, depending on risk factors for severe anaphylaxis. Following an anaphylactic reaction, management should focus on developing an emergency action plan, referral to an allergist, and patient education on avoidance of triggers and appropriate use of an epinephrine auto-injector.

Anaphylaxis is a severe allergic reaction that occurs quickly and can be fatal. The incidence of anaphylaxis in the United States between 2004 and 2016 was 2.1 per 1,000 person-years, with one-fourth of anaphylactic reactions affecting children younger than 17 years. 1 Most anaphylactic reactions occur outside the hospital setting ( Table 1 ) , 2 , 3 and most individuals go to the hospital or emergency department for treatment. 2 , 4 In the United States, the incidence of anaphylaxis peaks in children two to 12 years of age and in adults between 50 and 69 years of age. 1 One out of 20 of all anaphylaxis cases may require hospitalization 1 , 2 ; in the United States, hospitalizations for anaphylaxis have steadily increased over the past 10 years. 5 The annual number of confirmed anaphylaxis-related deaths in the United States ranges from 186 to 225. 5 The average fatality rate is 0.3% for most hospitalizations or emergency department presentations for anaphylaxis. 5 Risk factors for severe or fatal anaphylaxis include coexisting asthma, mast cell disorders, age older than 50 years, underlying cardiovascular disease, peanut and tree nut allergy, and drug-induced reactions. 6 – 10

WHAT'S NEW ON THIS TOPIC

One out of 20 of all anaphylaxis cases requires hospitalization; in the United States, hospitalizations for anaphylaxis have steadily increased over the past 10 years.

Gastrointestinal and respiratory symptoms of anaphylaxis are more likely to be overlooked in children. Only 55% of health care professionals recognize anaphylaxis without cutaneous involvement.

One-half of patients presenting to the emergency department who meet the National Institute of Allergy and Infectious Diseases/Food Allergy and Anaphylaxis Network diagnostic criteria for anaphylaxis receive treatment with epinephrine.

Pathophysiology

There are two types of anaphylactic reactions: immunoglobulin E (IgE) mediated and nonimmune (i.e., direct activation). 11 Most cases of anaphylaxis are IgE mediated in which antibodies to a particular allergen activate mast cells and basophils, resulting in degranulation and release of a wide variety of chemical mediators. Nonimmune anaphylaxis occurs by direct activation of mast cell and basophil receptors or complement-mediated activation. Distinction between the two types is not clinically possible, and treatment is the same for both. 11

Clinicians should be familiar with the differential diagnosis of anaphylaxis because many other conditions can present with signs or symptoms of anaphylaxis ( Table 2 11 , 12 ) . Signs and symptoms of an allergic reaction typically occur within one to two hours of exposure to an allergen, usually within 30 minutes for a food allergy and faster for parenteral medication or insect stings. Most acute allergic reactions are mild and self-limited, involving a single organ system, often the skin, with symptoms such as swelling of the lips or face, hives or welts, or tingling of the mouth. Anaphylaxis is distinguished from a mild or moderate allergic reaction by the sudden involvement of two or more organ systems manifesting with a variety of symptoms such as difficulty breathing, swelling of the tongue, swelling or tightness in the throat, wheezing, sudden persistent cough, abdominal pain, vomiting, and hypotension 13 ( Table 3 14 ) . Anaphylaxis can also be diagnosed by the isolated involvement of the cardiovascular system in the setting of hypotension or cardiovascular collapse after exposure to a known allergen. 14 Although isolated hypotension is a rare presentation of anaphylaxis, it often results in hospitalization and can be a marker of severity. 15

Making an accurate diagnosis is important because epinephrine is administered more often to patients diagnosed with anaphylaxis. 16 , 17 Clinicians must be familiar with and recognize the wide spectrum of presentations to avoid a missed diagnosis ( Table 4 2 , 4 , 16 , 18 – 22 ) . For example, syncope and hypotension are more common presentations in drug-induced anaphylaxis, 7 and in children, gastrointestinal and respiratory symptoms are more likely to be overlooked despite the more common occurrence of gastrointestinal symptoms. 18 , 23 In one study, only 55% of health care professionals recognized anaphylaxis without cutaneous involvement. 24

LABORATORY TESTING

Serum tryptase levels reflect mast cell degranulation and peak one to one and a half hours after the onset of anaphylaxis. Their testing availability limits the feasibility of measuring serum tryptase in an acute setting, and the treatment of a patient with possible anaphylaxis should not be based on serum tryptase levels alone. 25 If a diagnosis of anaphylaxis is in doubt, results of laboratory testing up to three hours after symptom onset can support the diagnosis in some patients 26 ; however, levels are often normal in food-triggered reactions. 10 , 11

The most common causes of anaphylaxis are foods, medications, and stinging insect venom. However, there are a wide range of specific triggers ( Table 5 2 , 4 , 6 , 7 , 18 , 27 – 29 ) , and the frequency varies with age and geographic region. 18 – 20 , 27 In the United States, food-triggered anaphylaxis is most common in children from birth to four years of age, whereas anaphylaxis to medications is more common in adults 50 years and older. 21 , 30 , 31

Clinicians and patients do not always correctly identify the causative agent. 16 Referral of patients with an anaphylactic reaction for allergy testing may help determine the offending trigger. Idiopathic triggers occur in up to 20% of anaphylactic cases, and identifying the trigger of an anaphylactic episode is not always possible. 5 , 9 , 18 , 32

Management of Anaphylaxis

Epinephrine.

The mainstay of treatment of acute IgE-mediated or nonimmune anaphylaxis is epinephrine ( Figure 1 8 , 10 , 11 , 13 , 21 , 26 , 33 – 36 ) . Epinephrine causes an increase in peripheral vascular resistance plus inotropic and chronotropic cardiac effects, leading to an increase in blood pressure. It causes bronchodilation and decreased mucosal edema through the vasodilation of the skeletal and smooth muscles in the airways and stabilization of mast cells and basophils.

The onset of action of epinephrine is usually three to five minutes, and intramuscular administration into the anterolateral thigh is the preferred route. 8 , 10 , 25 , 26 , 33 , 34 Epinephrine auto-injectors can be used in health care settings and are advantageous because they are quicker to administer and decrease dosing errors. 26 At recommended doses, the most common adverse effects of epinephrine include agitation, anxiety, tremulousness, headache, dizziness, pallor, and palpitations. There are no absolute contraindications to administering epinephrine for anaphylaxis.

Delayed or lack of epinephrine use continues to be a problem despite current guidelines emphasizing the importance of early administration. 37 Retrospective studies show that approximately one-half of patients presenting to the emergency department who meet the National Institute of Allergy and Infectious Diseases/Food Allergy and Anaphylaxis Network diagnostic criteria for anaphylaxis receive treatment with epinephrine. 16 , 32 , 38 An initial injection of epinephrine before the patient arrives at the emergency department decreases the likelihood of hospital admission, 39 and not administering epinephrine to treat anaphylaxis is associated with worse outcomes and mortality. 33 , 34 Reasons for failure to use epinephrine include delayed presentation, 40 misdiagnosis as a mild or moderate allergic reaction, 16 , 19 , 32 and failure to use the National Institute of Allergy and Infectious Diseases/Food Allergy and Anaphylaxis Network diagnostic criteria. 15 , 41 Clinicians cannot predict whether an allergic reaction episode will rapidly progress; therefore, early use of epinephrine should be considered even with mild symptoms or single-system involvement. 8

HISTAMINE H1 AND H2 ANTAGONISTS AND CORTICOSTEROIDS

Antihistamines and corticosteroids are not effective first-line treatments for anaphylaxis. Guidelines recommend that antihistamines and corticosteroids be used only as an adjunct to epinephrine. 8 , 11 , 25 Antihistamines have an onset of action of one to two hours. Although they improve cutaneous erythema and decrease pruritus, they have not been shown to reverse upper airway obstruction or improve hypotension. 42 The onset of action for corticosteroids is approximately six hours; therefore, they have little to no effect on initial signs and symptoms of anaphylaxis. A systematic review of corticosteroid use in the management of anaphylaxis was inconclusive for the reduction of biphasic reactions; however, corticosteroids may decrease the length of hospital stay. 43

BETA 2 AGONISTS AND GLUCAGON

Beta 2 agonists are used for the treatment of patients with reactive airways disease or any patient presenting with signs of active bronchospasm. 8 , 25 Any patient with refractory hypotension, especially those being treated with beta blockers, should be given glucagon because it has inotropic and chronotropic effects that are not mediated through beta receptors. 8 , 13 , 25

INTRAVENOUS FLUIDS AND OXYGEN THERAPY

Oxygen should be administered to patients presenting with respiratory symptoms, decreased oxygen saturation, or hypotension. 8 During anaphylaxis, vascular dilation and increased permeability can lead to intravascular fluid shifting into the extravascular space, resulting in distributive shock. Therefore, it is essential to establish two large-bore intravenous access sites and administer fluids when signs or symptoms of shock occur ( Figure 1 8 , 10 , 11 , 13 , 21 , 26 , 33 – 36 ) . Placing a patient with hypotension in a recumbent position with the lower extremities raised is preferred to elevating the head, even if the patient has an upper airway obstruction. 8 , 35

TRANSFER TO HIGHER LEVEL OF CARE

Patients should be transported to the hospital for continued therapy and monitoring, especially those with an initial presentation of significant respiratory or circulator y compromise, and patients with refractory anaphylaxis. Refractory anaphylaxis occurs in patients who do not respond to initial treatment with epinephrine, supplemental oxygen, intravenous fluid resuscitation, and second-line medications.

Observation Period

Biphasic reactions occur in less than 5% of patients diagnosed with anaphylaxis 2 , 44 and are defined as the recurrence of anaphylaxis within 72 hours of the initial reaction without reexposure to the allergen. A recent meta-analysis showed that an observation time greater than six hours after resolution of anaphylactic symptoms could exclude the recurrence of a secondary reaction in more than 95% of patients. 45 A minimum observation period of four hours supports current guidelines, with longer observation periods recommended based on individualized factors such as previous biphasic reaction, severity of initial presentation, treatment with multiple doses of epinephrine, a previously protracted anaphylactic reaction, unknown anaphylactic trigger, or presence of risk factors for severe or fatal anaphylaxis. 8 , 11 , 25 , 44 , 46

Post-Anaphylaxis Care

Anaphylaxis action plan.

All patients at risk of anaphylaxis should be provided with an action plan instructing them on how to manage an episode of anaphylaxis, including the proper administration of epinephrine. 8 , 11 , 25 , 47 Parents of at-risk children, especially children with a documented food allergy who attend school, preschool, or childcare, should share the action plan with the staff caring for their children. 47 The action plan should include documentation of confirmed allergens, signs and symptoms of anaphylaxis, an emphasis on epinephrine as the first-line treatment, the first aid response, identification of the child including a photo, and parent or guardian contact information. An example plan is available at https://www.healthychildren.org/SiteCollectionDocuments/AAP_Allergy_and_Anaphylaxis_Emergency_Plan.pdf . Preventive measures to decrease the risk of repeat episodes of anaphylaxis are listed in eTable A .

EPINEPHRINE AUTO-INJECTOR PRESCRIPTION

Epinephrine auto-injectors are safe when used correctly. Guidelines recommend that all patients diagnosed with an anaphylactic reaction be prescribed an auto-injector. Patients treated in the emergency department for anaphylaxis commonly do not receive a prescription when they are discharged. 48 Patients do not always fill the prescription, even when it is offered, 49 or carry the epinephrine auto-injectors with them at all times. 50 , 51 Common reasons patients do not comply with treatment include thinking that they will not be exposed to the allergen or that their symptoms are not severe enough, that they have never had to use the auto-injector before, and that they either forget or do not feel a need to carry it with them at all times. 50 Auto-injectors can be expensive and often have a one-year expiration date, requiring an annual purchase of one or more. Effective patient education during examinations should emphasize the importance of keeping the auto-injector available for immediate use.

ALLERGIST REFERRAL

Referral to an allergist is appropriate if a clinician feels inadequately trained to provide education or if the patient presents after the reaction and the offending agent cannot be confirmed. 8 , 25 Allergists should obtain a detailed patient history, coordinate additional outpatient testing, offer additional allergen avoidance counseling, and provide the patient with medical alert or identification jewelry.

This article updates previous articles on this topic by Arnold and Williams , 36 and Tang . 12

Data Sources: A PubMed search was completed using the key terms anaphylaxis, epinephrine, antihistamine, corticosteroids, glucagon, management, epidemiology, diagnosis, biphasic, and fatal. The search included meta-analyses, systematic reviews, practice guidelines, clinical trials, and original studies. Also searched were the Cochrane database, ECRI Guidelines Trust, Essential Evidence Plus, and the U.S. Preventive Services Task Force. Search dates: August 28, 2019, and April 29, 2020.

The views expressed in this article are those of the authors and do not reflect the official policy or position of the Department of the Army, Department of the Navy, Department of the Air Force, Uniformed Services University of the Health Sciences, Department of Defense, or the U.S. government.

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Food Allergies Clinical Presentation

• Author: Elizabeth A Secord, MD; Chief Editor: Michael A Kaliner, MD  more...
• Sections Food Allergies
• Practice Essentials
• Pathophysiology
• Epidemiology
• Non-IgE-Mediated Food Allergies
• Cross-Reactivity Food Allergy Syndromes
• Food-dependent Exercise-induced Anaphylaxis
• Patient Education
• History and Physical Examination
• Physical Examination
• Complications
• Approach Considerations
• Serum Studies
• Elimination Diet
• Skin Testing
• Food Challenge Confirmation of Food Allergy
• Emergency Plan
• Emergency Medications
• Pharmacologic Therapies
• Consultations
• Medication Summary
• Alpha/Beta Adrenergic Agonists
• Antihistamines
• Monoclonal Antibodies, Anti-asthmatics
• Immunotherapy
• Allergen-Specific Immunotherapy
• Questions & Answers

Signs and symptoms

IgE-mediated reactions

Signs and symptoms of IgE-mediated reactions including anaphylaxis, which is a rapidly progressive, life-threatening reaction. Other signs and symptoms may include the following: 

Oropharyngeal pruritus

Angioedema (eg, laryngeal edema)

Abdominal pain

Ocular injection, ocular pruritus, conjunctival edema, periocular swelling

Nasal congestion, nasal pruritus, rhinorrhea, and sneezing

Feeling of impending doom

Cardiovascular symptoms including hypotension, cardiac arrhythmias, and cardiac arrest can be associated with anaphylaxis. [ 6 ]

Oral allergy syndrome/pollen food allergy syndrome (OAS/PFAS)

• Allergic rhinitis, conjunctivitis and asthma symptoms with pollen exposure associated with oropharyngeal pruritis after exposure to raw fruits, vegetables and sometimes nuts that cross react with sensitizing pollen [ 7 ]

Food protein-induced enterocolitis (FPIES) [ 8 , 9 ]

Weight loss

Dehydration and hypovolemia

Milk protein-induced proctocolitis (infants) [ 8 , 9 , 10 ]

Blood and mucous in stool 

Poor weight gain or weight loss

Eosinophilic gut disease [ 11 ]

Dependent on areas of gut where eosinophilic infiltration is present

Esophageal disease results in reflux, weight loss, failure to thrive, difficulty swallowing, and food impaction

Gastrointestinal disease results in nausea, vomiting, diarrhea, and weight loss

Food-induced anaphylaxis

Cardiovascular collapse

Medical history

Necessary elements of a thorough medical history include the following:

Complete list of all foods suspected of causing symptoms (including foods and food additives listed on prepared food labels)

Manner in which the food was prepared (cooked, raw, added ingredients)

Minimum quantity of food exposure required to cause the symptoms

Reproducibility of symptoms on exposure to the food

Exercise after ingestion but prior to reaction to elicit possible food-dependent, exercise-induced anaphylaxis [ 12 ]

Personal or family history of other allergic disease 

Factors that can potentiate a food-allergic reaction (eg, exercise, [ 13 ]  nonsteroidal anti-inflammatory drugs [NSAIDs], or alcohol) [ 12 ]

In addition, obtain a thorough description of each reaction, including the following:

Route of exposure (ingestion, skin contact (especially in patients with atopic dermatitis) [ 14 , 15 , 16 ]  and inhalation) and dose

Timing of symptom onset in relation to food exposure (IgE reactions usually occur very soon after ingestion, other reactions slower onset)

All observed symptoms and each one’s severity

Duration of the reaction

Treatment provided and clinical response to treatment

Most recent reaction

Physical examination findings are most useful for the following:

Skin: urticaria and angioedema 

Lungs: wheezing

Cardiovascular: assess for signs of vasodilation and shock (hypotension, tachycardia)

Assess for dehydration especially if there are GI symptoms (mucous membranes, capillary refill, skin turgor, weight if patient stable enough to obtain)

Assessing nutritional status, growth parameters, and signs of other allergic disease, especially in children

Complications of food protein-induced enterocolitis syndrome (FPIES), milk-induced proctocolitis, and eosinophilic gut diseases include weight loss and failure to thrive.

Eosinophilic esophagitis can cause difficulty swallowing, food impaction, and strictures.

All food allergies can lead to anxiety and food avoidance issues, which may require counseling.

Anaphylaxis can lead to death.

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Contributor Information and Disclosures

Elizabeth A Secord, MD Professor (Clinical), Division Chief of Allergy and Immunology, Medical Director of Horizons Project for Pediatric and Adolescent HIV Treatment and Prevention, Director, Primary Immune Deficiency Clinic, Department of Pediatrics, Wayne State University School of Medicine; Physician, Division of Allergy, Immunology and Rheumatology, Children's Hospital of Michigan (Detroit Medical Center) Elizabeth A Secord, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology , American Academy of Pediatrics , American College of Allergy, Asthma and Immunology , American Medical Association , Clinical Immunology Society , Michigan Allergy and Asthma Society Disclosure: Received research grant from: Novavax; pfizer; gilead.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Received salary from Medscape for employment. for: Medscape.

Michael A Kaliner, MD Clinical Professor of Medicine, George Washington University School of Medicine; Medical Director, Institute for Asthma and Allergy Michael A Kaliner, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology , American Association of Immunologists , American College of Allergy, Asthma and Immunology , American Society for Clinical Investigation , American Thoracic Society , Association of American Physicians Disclosure: Nothing to disclose.

Scott H Sicherer, MD Professor of Pediatrics, Jaffe Food Allergy Institute, Mount Sinai School of Medicine of New York University Scott H Sicherer, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology , American Academy of Pediatrics Disclosure: Nothing to disclose.

Dan Atkins, MD Assistant Professor, Department of Pediatrics, University of Colorado Health Sciences Center; Head, Division of Ambulatory Pediatrics, Department of Pediatrics, Director, Pediatric Day Program, National Jewish Medical and Research Center

Dan Atkins, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology and American Thoracic Society

Disclosure: Nothing to disclose.

Stephen C Dreskin, MD, PhD Professor of Medicine, Departments of Internal Medicine, Director of Allergy, Asthma, and Immunology Practice, University of Colorado Health Sciences Center

Stephen C Dreskin, MD, PhD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology , American Association for the Advancement of Science , American Association of Immunologists , American College of Allergy, Asthma and Immunology , Clinical Immunology Society , and Joint Council of Allergy, Asthma and Immunology

Disclosure: Genentech Consulting fee Consulting; American Health Insurance Plans Consulting fee Consulting; Johns Hopkins School of Public Health Consulting fee Consulting; Array BioPharma Consulting fee Consulting

John M James, MD Consulting Staff, Department of Pediatrics, Department of Allergy and Immunology, Colorado Allergy and Asthma Centers, PC

John M James, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American College of Allergy, Asthma and Immunology, American Medical Association, Colorado Medical Society, and Phi Beta Kappa

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Volume 1 Supplement 1

Food Allergy and Anaphylaxis Meeting 2011

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Diagnosis and management of food-induced anaphylaxis

• Dana Wallace 1  

Clinical and Translational Allergy volume  1 , Article number:  S64 ( 2011 ) Cite this article

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Anaphylaxis is an acute, life-threatening, systemic reaction with varied clinical presentations and severity that results from the systemic release of mediators from mast cells and basophils. The diagnosis of food-induced anaphylaxis is based on a combination of medical history and presence of specific IgE to the responsible food. In general, the more rapid the onset of symptoms following exposure to the allergen, the more likely the reaction will be severe and life threatening. However when ingested food is the allergen, it may take up to 25 minutes from onset of anaphylaxis to cardiopulmonary arrest, making the diagnosis even more challenging. In food-induced, fatal anaphylaxis episodes up to 80% are not associated with cutaneous signs or symptoms, the signal that most patients will recognize first. Furthermore, it is well established that patients with food-induced anaphylaxis under utilize epinephrine. Thus, ongoing education for the patient who is at risk for anaphylaxis becomes essential.

While occurrences of food allergy are believed to be increasing, the true prevalence is unknown. Food allergies are highest in children and adolescents and are thought to be the most common cause of anaphylaxis in the outpatient setting, accounting for approximately 30% of fatal reactions. Fatalities from food-induced anaphylaxis are highest in teenagers and young adults, among those with asthma, and in cases when there has been a delay in the administration of epinephrine. Biphasic reactions occur in approximately 25% of fatal and near-fatal, food-induced anaphylaxis events. Special circumstances involving food allergy that will be discussed include exercise-induced anaphylaxis, unsuspecting hidden food allergy, and the significance of food allergy for vaccine administration.

The treatment of anaphylaxis involves the immediately administration of epinephrine. When there is any doubt about the diagnosis, it is generally best to administer epinephrine rather than waiting for more severe symptoms. In the treatment of food-induced anaphylaxis, more than a single dose of epinephrine may be required; these doses can be given every 5-10 minutes, and a longer period of observation is recommended. While IM administration is preferred by many national and international guidelines, the controversy over IM vs. subcutaneous epinephrine use will be discussed. Following the administration of epinephrine, other treatment modalities include 1) placing the patient in a supine position, 2) oxygen, and 3) fluid replacement. The role of the second line, supportive medications including H1 and H2 antihistamines and corticosteroids has not been established for the treatment of acute, biphasic, or prolonged anaphylaxis. Glucagon may be considered in patients taking a beta-blocker who are not responding to epinephrine.

Physicians and office staff need to maintain clinical proficiency in anaphylaxis management, which should include an established written plan to deal with anaphylaxis and regular practice sessions. An action plan for the diagnosis and management of food-induced anaphylaxis should be provided to every patient with food allergies. A review of the action plan and technique for auto-injection of epinephrine should occur at regularly scheduled office visits. Recognizing that at the present time, there is no way to prevent food-induced anaphylaxis other than by avoiding the food. the patient requires frequent reinforcement that epinephrine, NOT antihistamines, is the only effective medication for the treatment of anaphylaxis and that a delay in administration is associated with more severe symptoms and a higher rate of fatality. Every patient with food-induced anaphylaxis must always have at least two doses of auto-injectable epinephrine immediately available.

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Wallace, D. Diagnosis and management of food-induced anaphylaxis. Clin Transl Allergy 1 (Suppl 1), S64 (2011). https://doi.org/10.1186/2045-7022-1-S1-S64

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Signs and Symptoms of Food Allergy and Food-Induced Anaphylaxis

Affiliations.

• 1 Division of Allergy and Immunology, Children's National Health System, George Washington University School of Medicine and Health Sciences, Washington, DC, USA. Electronic address: [email protected].
• 2 Division of Allergy and Immunology, Children's National Health System, George Washington University School of Medicine and Health Sciences, Washington, DC, USA.
• PMID: 26456438
• DOI: 10.1016/j.pcl.2015.07.008

Food allergies are increasing in prevalence. In order for pediatric clinicians to appropriately diagnose and manage food allergies, the characteristic signs and symptoms of these potentially severe reactions must be recognized. Unlike nonimmunologic adverse food reactions (such as lactose intolerance and food poisoning), food allergies by definition are immune-mediated responses that occur reproducibly on food ingestion. The varying clinical presentations of food allergy include IgE-mediated disorders, mixed IgE- and cell-mediated disorders, and cell-mediated food allergies. This review describes the clinical manifestations of each of these categories of food allergy, with special emphasis on recognition of food-induced anaphylaxis.

Keywords: Anaphylaxis; Food allergy; History; Presentation; Symptoms.

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A food allergy powerhouse: Northwestern’s Global Food Allergy Prevention Summit 2024

By Maggie Goldman, Julia Valaika, and Cate Weiser July 9, 2024

Northwestern University’s Center for Food Allergy and Asthma Research (CFAAR) hosted its second annual Global Food Allergy Prevention Summit (GFAPS) this month, drawing clinicians and researchers from around the world to strategize the future of food allergy prevention research.

This year’s summit, held from June 30 to July 2, expanded its focus by offering three distinct sections: the Pediatric Food Allergy Care Conference (PFACC), the Summit for Advancing Equity in Food Allergy (SAEFA), and GFAPS workshops. That growth was spurred largely by the overwhelmingly positive response to last year’s event, with participants eager to maximize the summit’s unique collaborative structure.

Ruchi S. Gupta, MD, MPH , director of CFAAR and professor of pediatrics at the University Feinberg School of Medicine, welcomed attendees and emphasized the need for international collaboration to shift the paradigm on food allergy prevention.

“Food allergy impacts 32 million Americans, about one in ten adults and one in thirteen children,” said Gupta. “Those people are the reason we’re here — to work together, gain knowledge, and share ideas about how we can make the world better for each and every one of them. We’re here to move the needle on prevention and change the course of food allergy.”

Food allergy impacts 32 million Americans, about one in ten adults and one in thirteen children. Those people are the reason we’re here.”

Attendees travelled from as far as India, Australia, England to participate in the event, offering their perspectives as allergists, pediatric care providers, researchers, industry partners, and patient advocates.

Alkis Togias, MD , chief of the Allergy, Asthma and Airway Biology branch at the National Institute of Allergy and Infectious Diseases (NIAID), gave a welcoming address, underscoring the urgency of the summit’s mission.

“This summit has become such an important event for this field,” said Togias. “To be able to meet and discuss and offer ideas about advancing allergy prevention research—that’s endlessly valuable.”

Each of the three conferences offered a different experience for attendees, with the first two (SAEFA and PFACC) holding traditional seminars. In contrast, GFAPS organized a day of intense workshops where guests designed and then proposed five new studies. The six working groups focused on aspects considered essential to transforming food allergy prevention:

• Early dietary influences on food allergy development
• Molecular mechanisms of food allergy prevention
• Influences on gut microbiome
• Skin: barrier or pathway to food allergy development
• Early treatment and secondary prevention
• Environmental Factors

The groups returned the following day with several research questions and strategies for answering each. Those questions included:

• “Is triple exposure (breastfeeding, maternal allergen consumption during breastfeeding, and early introduction in infancy) associated with a greater reduction of food allergies to peanuts, eggs, and milk?”
• “What are the best educational resources about food allergies for clinicians and parents? Do those resources change community behavior as a whole?”
• "What are the prenatal environment risk factors associated with the development of food allergies in children, and to what extent do maternal diet, maternal health, and environmental exposures contribute to the risk?”

The overarching idea throughout the six presentations was the necessity for researchers in food allergy and other fields to collaborate.

“Harmonization is necessary, leveraging data from different studies is necessary — harmonizing that data with what we have in food allergy would be wonderful,” said Amal H. Assa'ad, MD , associate director of Allergy and Immunology at Cincinnati Children’s Hospital.

A paper summarizing the group’s findings is currently being drafted and is expected to be published in the coming months.

Summit for Advancing Equity in Food Allergy (SAEFA)

The second section of this year’s summit showcased a series of conversations on health equity, each exploring first barriers and strategies to managing food allergies. By aligning shared goals from the many perspectives of payors, clinicians, policymakers, patients, and other innovators, the discussions aimed to address the proposed key issues and create a roadmap forward. Talks unfolded across four consecutive panels: daily life, prevention, diagnosis and treatment of food allergy.

To kick off the summit, Ajanta Patel, MD , director of Chronic Disease Prevention and Health Promotion at the Chicago Department of Public Health, spoke about health equity, emphasizing that it is “a shared opportunity, not a shared challenge.”

The first session of the day, the Daily Life panel, identified key barriers to achieving health equity in food allergy management and proposed improvement strategies. Panelists discussed access to affordable allergen-free foods, time as a resource, the mental health effects of food allergy, and equal access to epinephrine and other medications.

One panelist Zacky Munoz , a 12-year-old author and food allergy activist, energetically highlighted the varied understanding of food allergies and their severity.

“As a kid, we rely on other individuals to take care of us,” Munoz said. “However, there is not a lot of education on this.”

The panel agreed on the roadmap for improvement from this panel to include better education, refined diagnosis and quality measures, and large studies for data-driven policies.

Following talks included the Prevention Panel, which featured a group of 8 experts, including industry partners, payors, clinicians and researchers. Part of their conversation focused on Medicaid's crucial role in covering prevention efforts and barriers, such as insurers demanding quick returns on investment, which are unrealistic with infant interventions. Extra emphasis was given to the need for research to demonstrate the long-term economic benefits, with calls to “start doing the research that defines the outcome” to prove the value of these early interventions.

Moderator Waheeda Samady, MD , associate professor of pediatrics at Northwestern, reiterated that imperative.

“Do the studies so that Medicaid will start supporting prevention work,” Samady said.

Although food allergies affect approximately 8% of children, less than 1% of Medicaid-enrolled children have a formal diagnosis. With only half of U.S. allergists accepting Medicaid patients, access to diagnostic services and specialists is a significant barrier. The summit aimed to reduce these barriers by advocating for increased access to allergists and additional training for pediatricians in food allergy diagnosis.

Pediatric allergist Sai R Nimmagadda, MD , associate professor of pediatrics at Northwestern, noted that, in his experience, wait times to see a specialist are due to a lack of both space and time. The panel discussed strategies that included using mobile vans to improve access and increase care in rural areas, which are particularly vulnerable to fatal anaphylaxis due to distance from care.

The final panel of the summit discussed several barriers and strategies towards equitable food allergy treatment. Panelists acknowledged that a lack of diverse allergists had led to cultural misunderstandings and mistrust, and language barriers often complicate reading food labels and navigating health insurance decisions.

Jessica M. Palmieri, DO , assistant professor of pediatrics at Northwestern highlighted that income level greatly influences families' education about the newest treatment options such as oral immunotherapy.

Emily Brown, CEO of Attane Health, stated that “treatment must be a ‘both and,’” underscoring that food and nutrition care is as critical as the emerging technologies, bringing a focus back to the intersection of food insecurity and food allergy.

Pediatric Food Allergy Care Conference (PFACC)

The Pediatric Food Allergy Care Conference gathered pediatricians, primary care providers, researchers and advocates for a day of presentations centered on the latest guidance and research on pediatric allergies. Subjects included allergy prevention, management, treatment and patient education.

Gupta welcomed the attendees and urged them to “foster a network of support and collaboration that extends beyond the conference and into practices to improve outcomes for patients and greater communities.”

Michelle Barnes, MD, FAAP , president of the Illinois chapter of the American Academy of Pediatrics and Professor of Clinical Pediatrics and Internal Medicine at the University of Illinois, delivered a morning keynote, speaking on pediatricians' role in food allergy care.

“As we stand at the forefront of children’s healthcare, our responsibilities extend far beyond diagnosis and treatment,” said Barnes. “We are the guardians of our patients’ overall well-being, their advocates, and the first line of defense against the multifaceted obstacles they encounter.”

As we stand at the forefront of children’s healthcare, our responsibilities extend far beyond diagnosis and treatment.”

Barnes also cited the conference as a testament to the pediatric community’s commitment to advancing knowledge and improving care for children with allergies, asthma, and related conditions.

The talks, geared primarily towards primary care providers, covered a range of clinical-centric topics, including diagnostics and testing, condition management, and recent changes in treatment.

Togias, who spoke throughout the weekend, shared news on NIAID efforts and noted that Learning Early About Peanut (LEAP) was a “major breakthrough” in the world of food allergy. LEAP is a treatment protocol based on findings from a 2015 study that showed early childhood exposure to peanuts decreased the risk of developing peanut allergy.

In addition to prevention, speakers highlighted recent treatments. Palmieri, who also spoke during SAEFA, outlined appropriate ways to mediate a food allergy reaction, as well as how to recognize anaphylaxis, establishing epinephrine as first-line treatment in the case two or more body systems are reacting, and the use of antihistamines as second-line treatment.

Melissa Engel, a clinical psychology PhD student at Emory University, concluded the day with her presentation, “Psychosocial Aspects of Pediatric Food Allergy.” Engel addressed psychosocial challenges in individuals with food allergies, drawing from peer-reviewed research and patient narratives to show the psychological burden often felt by those with food allergies, including heightened anxiety and depressive symptoms.

“‘No one understands that if you have multiple severe food allergies, you lose all spontaneity,’” Engel said, quoting a study respondent. “‘You become a planner by force.’ Striking the right balance between education and adaptive caution is crucial for the well-being of patients with food allergy.”

Following the day’s talks, guests were encouraged to utilize the resources on the CFAAR website , which are designed to be shared with patients and their families and are available in multiple languages. Those resources include a food allergy passport, an emergency action plan template, food label workbooks, and tip sheets.

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• Published: 28 June 2024

A potentially lifesaving error: unintentional high-dose adrenaline administration in anaphylaxis-induced cardiac arrest; a case report

• Felix Patricius Hans 1 ,
• Leo Benning 1 ,
• Jan-Steffen Pooth 1 &
• Hans-Jörg Busch 1  

International Journal of Emergency Medicine volume  17 , Article number:  78 ( 2024 ) Cite this article

275 Accesses

Metrics details

Cardiopulmonary resuscitation is a crucial skill for emergency medical services. As high-risk-low-frequency events pose an immense mental load to providers, concepts of crew resource management, non-technical skills and the science of human errors are intended to prepare healthcare providers for high-pressure situations. However, medical errors occur, and organizations and institutions face the challenge of providing a blame-free error culture to achieve continuous improvement by avoiding similar errors in the future. In this case, we report a critical medical error during an anaphylaxis-associated cardiac arrest, its handling and the unexpected yet favourable outcome for the patient.

Case presentation

During an out-of-hospital cardiac arrest due to chemotherapy-induced anaphylaxis, a patient received a 10-fold dose of epinephrine due to shortcomings in communication and standardization via a central venous port catheter. The patient converted from a non-shockable rhythm into a pulseless ventricular tachycardia and subsequently into ventricular fibrillation. The patient was cardioverted and defibrillated and had a return of spontaneous circulation with profound hypotension only 6 min after the administration of 10 mg epinephrine. The patient survived without any residues or neurological impairment.

Conclusions

This case demonstrates the potential deleterious effects of shortcomings in communication and deviation from standard protocols, especially in emergencies. Here, precise instructions, closed-loop communication and unambiguous labelling of syringes would probably have avoided the epinephrine overdose central to this case. Interestingly, this serious error may have saved the patient’s life, as it led to the development of a shockable rhythm. Furthermore, as the patient was still in profound hypotension after administering 10 mg of epinephrine, this high dose might have counteracted the severe vasoplegic state in anaphylaxis-associated cardiac arrest. Lastly, as the patient was receiving care for advanced malignancy, the likelihood of termination of resuscitation in the initial non-shockable cardiac arrest was significant and possibly averted by the medication error.

Sudden cardiac death is among the top three leading causes of death in developed countries. Emergency medical service (EMS) providers treat between 28 and 244 cardiac arrests per 100,000 inhabitants per year as out-of-hospital cardiac arrests (OHCA) worldwide [ 1 ]. In-hospital cardiac arrest (IHCA), at the same time, is a relevant driver of mortality in admitted patients, with an incidence of 1.5 patients per 1,000 [ 2 ]. Anaphylaxis-related cardiac arrests are highly infrequent events that occur in and out of hospitals (0,04/100,000 or 0.12% of OHCA) [ 3 , 4 ]. While anaphylaxis-associated OHCA is triggered mostly by insect stings and food [ 5 ], anaphylaxis-associated IHCA is mainly caused by contrast and chemotherapy agents [ 4 ].

Cardiopulmonary resuscitation (CPR) and advanced life support (ALS) are core skills on which acute care providers receive training [ 6 ]. Although highly standardized, CPR situations pose a challenge, especially to ad-hoc teams in hospitals or the field. Epinephrine is among the crucial medications in both anaphylaxis and cardiac arrest. However, the dosage and route of application significantly differ depending on the clinical state. As a result, barriers to administering adequate doses of epinephrine frequently potentially result in deleterious under- and overdosing of epinephrine [ 7 , 8 , 9 , 10 ]. In states of anaphylactic shock, driven by fluid extravasation and vasodilation, the second-line therapy after epinephrine is the administration of crystalloid fluids (0.5–5 l) [ 11 ].

Crew resource management (CRM) and the analysis of human factors deal with the nature of human perception in high-pressure environments, the laws of communication and with the science of medical errors [ 12 , 13 ]. Therefore, CRM elements are crucial in clinical and preclinical algorithms to ensure the best possible quality of care, especially in high-risk-low-frequency events like cardiac arrests [ 14 ]. Often, an error occurs from the convergence of multiple contributing factors and may harm patients (immediate effect of wrong or missed action) as well as health care providers (disciplinary action, blame, loss of trust, job leave) [ 15 ]. Environments with underdeveloped institutional handling of errors may lead to underreporting of mishaps, near-misses and errors, fostering an even more harmful environment for patients [ 16 ]. Improving communication and medication safety, therefore, is among the ten goals of the Joint Commission for Patient Safety [ 15 , 17 , 18 ].

Here, we report the case of an anaphylaxis-associated OHCA in an oncologic private practice, where a severe medication error occurred due to shortcomings in communication and standardization. Despite this error, the patient had a favourable outcome and could consent to the case presentation. The report is drafted according to the CARE reporting guideline [ 19 ].

A 66-year-old woman was treated in an outpatient clinic/private practice for uterine serous carcinoma. On that day, the second dose of paclitaxel was scheduled to be administered via a venous port catheter system after an initial dose was administered 21 days before without any complications. A blood sample drawn before the start of the paclitaxel therapy showed no abnormalities except mild anemia (10.8 g/dl). On a routine basis, the patient received 20 mg of dexamethasone p.o., 150 mg of ranitidine p.o. and 2 mg of clemastine fumarate i.v. via the port catheter system. Subsequently, the nursing staff started a drip of 266 mg of paxlitaxel. The patient complained about shortness of breath (SOB) and nausea 10 min into the therapy. The oncologist was called to the patient and administered another 20 mg of dexamethasone i.v. and another push dose of 2 mg clemastine fumarate i.v. via the port catheter system. The patient was then transferred to a separate cubicle with a stretcher.

Upon arrival in the cubicle, the patient remained awake and still complained about SOB and nausea. The outpatient clinic’s team administered oxygen and called the emergency dispatch under the impression of an anaphylactic shock. In Germany, the EMS are dispatched in a rendezvous system with a doctor’s vehicle, which will assist in special circumstances by bringing a pre-hospital emergency physician to the site of an accident or illness [ 20 , 21 ]. In this case, an emergency physician was dispatched together with an ambulance to the code “anaphylaxis”. By that time, the patient had a loss of peripheral pulses, lost consciousness and had a non-invasive blood pressure (NIBP) of 60/40mmHg. An epinephrine drip was prepared by the outpatient clinic (of which the dose could not be determined in hindsight). Before the administration of the drip, the patient went into cardiac arrest (t = 0 min), and CPR was started immediately, as the outpatient clinic’s staff had coincidentally performed basic life support training the day before.

On arrival of the EMS (t = 8 min), the patient presented with a Glasgow Coma Scale (GCS) of 3, all vital signs absent under CPR from the outpatient clinic staff. EMS took over CPR and Bag-Mask-Ventilation (BMV) and attached a heart monitor (t = 8 min) showing a pulseless electrical activity (PEA: Brady-asystole with broad QRS complexes at a rate of approximately 10/min). According to ALS Guidelines, the team intended to apply 1 mg of epinephrine as a non-shockable rhythm was present [ 2 , 6 ]. As to the EMS it was unclear if the infusion connected to the patient’s port catheter system contained the potentially triggering substance, the drip was removed and replaced by 500 ml of a balanced crystalloid solution (t = 9 min). A 10 ml syringe was handed to the emergency physician, stating “Epinephrine is ready!”, and the epinephrine was administered via the port system (t = 10,5 min). The emergency physician returned the syringe to the paramedic, asking for “another milligram of epinephrine” to be administered within 3–5 min (according to ALS guidelines). The paramedic responded that he had just handed 10 mg in 10 ml to the emergency physician, and it became clear to the team that 10 mg of epinephrine had been applied directly to the port catheter. Almost immediately, the patient developed pulseless ventricular tachycardia (pVT). She received defibrillation with 200 J (biphasic, t = 12 min), and after 2 min of CPR, the patient was in ventricular fibrillation (vFib). After defibrillation with 200 J (biphasic, t = 14 min), the team performed a rhythm and pulse check after another 2 min of CPR and detected sinus tachycardia (136/min) and a central pulse (t = 16 min).

The return of spontaneous circulation (ROSC) was announced, and an evaluation according to the ABCDE mnemonic took place approximately 6 min after applying 10 mg of epinephrine. The patient presented with an open airway, ongoing BMV and a spontaneous respiratory rate of 14/min. End-tidal CO2 (etCO2) showed values of around 35mmHg, and NIBP showed profound hypotension (73/45 mmHg). Subsequent actions included the repetitive administration of norepinephrine push doses of 10 µg and endotracheal intubation (due to persistent GCS = 3; after administering 10 mg midazolam, 10 mg morphine and 20 mg etomidate).

Transport to the nearby cardiac arrest centre (CAC [ 22 ]) was uneventful. The patient was handed over to the cardiac arrest receiving team at t = 53 min. Norepinephrine (13 mcg/min) was administered with another 2000 ml of crystalloid fluids during the first 120 min after OHCA to counteract the persisting state of shock. A multi-region computer tomography (CT) revealed fractures of the costae 3–5 on the right and 3–6 on the left side with associated tension pneumothorax on the left side, which was decompressed with a chest tube in the emergency department. Cranial CT showed no abnormalities. Given the precise line of events, a normal ECG and only slightly elevated troponin T levels (67.1 ng/l) upon arrival, no coronary angiography was performed. According to local post-resuscitation care, outcome prediction after OHCA relies on cerebral imaging, CPR details (i.e. no-flow-time, underlying rhythm, etc.) and the biomarkers Neuron-Specific Enolase (NSE) and Serum S-100 β protein (S100), that were measured on arrival [ 23 , 24 ]. The NSE level was 47.6 µg/l, the S100 level was 5.730 µg/l, and the patient received cooling to 33 °C for 24 h. The maximum C - reactive protein was measured with 167.5 mg/ on day five after CPR, while aspiration pneumonia was treated with antibiotics (ampicillin/sulbactam).

Extubation took place after three days. The patient reported having nightmares for three days and hallucinations of black figures standing beside the bed. All symptoms eased on day four after extubation. The chest tube was removed on day five after CPR, and the patient was transferred to a primary hospital (closer to the patient’s home) after nine days in the intensive care unit (ICU). The primary hospital discharged the patient home after another six days of inpatient care without any residuals (Cerebral Performance Category (CPC) 1) except for newly diagnosed hypertension.

Discussion and conclusions

In the above case, an excessively high dose of epinephrine was directly administered through central venous access in a non-shockable OHCA that was considered anaphylaxis-associated and healthcare-related [ 2 ]. It is known that the incidence of anaphylaxis-associated cardiac arrest is very low [ 2 , 3 , 4 , 5 ] and that epinephrine may lead to higher rates of ROSC but does not foster beneficial neurological outcomes [ 25 ]. In this case, the conversion to a shockable rhythm, potentially induced by high-dose epinephrine, led to an immediate change of the ALS management, as the patient could be defibrillated as a result and had ROSC. Although it is widely accepted that shockable rhythms in cardiac arrest show higher survival rates and better CPC scores [ 26 , 27 ], no causation can be postulated, even if the administration of epinephrine was followed by immediate conversion of rhythm in this case. Nevertheless,, given the physiologic half-life of epinephrine between 3 and 20 min [ 28 , 29 ], the BP measured 6 min after the administration of 10 mg epinephrine via central venous access was surprisingly low with only 73/45 mmHg, indicating severe, persistent vasoplegic shock. The necessity of push doses of norepinephrine and administering 2.5 l of crystalloid fluids in the first 120 min after OHCA underscore this persistent state of shock. Yet, the discovered tension pneumothorax might have led to the development of an additional obstructive shock (due to chest compressions or ventilation) and, therefore, might have contributed to the persisting shock. In hindsight however, the high dose of epinephrine might have counteracted the shock states without causing relevant side effects.

Given the patient’s medical history with the respective clinical gestalt (advanced cancer state, therapy-associated BMI of 18 and hair loss), we assume that adherence to the guidelines by administering 1 mg of epinephrine might not have led to a ROSC after only 6 min. The EMS team would likely have considered an early termination of resuscitation (TOR) under those alternate circumstances.

In a structured debriefing following the CRM concept, the medical error was narrowed down to a divergence of standard dosages between the hospital environment and the local EMS. By standard, the physician in charge used epinephrine 1:10,000 (0.1 mg/ml), whereas the EMS standard concentration is 1:1,000 (1 mg/ml). Clearly, the emergency physician should have been aware of this fact and asked for a labelled syringe with a clear statement of the intended dose. This shortcoming led to the administration of a potentially harmful injection of an epinephrine overdose, which presumably saved the patient’s life in this case.

Given the descriptive nature of this work as a case report, the clear limitation is the lack of generalizability, and the finding does not imply a routine deviation from guidelines. Especially the previously described absence of clinical benefits from high doses of adrenalin in cardiac arrest [ 30 , 31 ] and its potentially harmful effects in anaphylaxis (i.e. myocardial infarction, pulmonary edema, death) [ 9 ] should lead to critically interpretating the events described here.

As the incidence of anaphylaxis-associated OHCA is very low [ 3 , 4 , 5 ] our case might nonetheless describe important findings on the topic. Firstly, the management of anaphylaxis is often characterized by inappropriate dosing and timing of epinephrine as a first-line medication [ 4 , 9 , 10 ]. This might indicate a need for high-fidelity simulation and training for anaphylaxis and CPR in special circumstances [ 2 , 32 ] and for organizational measures like standardization of code medications and prefilled or pre-labelled syringes [ 8 , 33 ]. Second, crew resource management elements (e.g. closed-loop communication, read-backs, call-outs) [ 32 , 33 ] should be a bedrock component in professional development for all healthcare workers. Additionally, these measures must be embedded in error-preventing environments on organizational levels [ 16 , 34 ]. As over two-thirds of anaphylaxis-associated IHCA occurred in malignancy patients [ 4 ], further research should systematically analyze the mechanisms and possible adaptations of guidelines in anaphylaxis-associated cardiac arrest to avoid premature TOR in those patients.

Data availability

No datasets were generated or analysed during the current study.

Abbreviations

Mask Ventilation

Cardiopulmonary Resuscitation

Return of Spontaneous Circulation

In-Hospital Cardiac Arrest

Intravenous

Out-Of-Hospital Cardiac Arrest

Termination of Resuscitation

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LB received funding through the Berta-Ottenstein-Programme for Clinician Scientists from the Faculty of Medicine, University of Freiburg.

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FPH consented the patient for publication and wrote the manuscript draft. LB substantively revised the draft and performed a literature review. JSP substantively revised the draft and performed a literature review. HJB substantively revised the draft, interpreted the data, and performed a literature review. All authors have approved the submitted version and have agreed both to be personally accountable for the author’s own contributions and to ensure that questions related to the accuracy or integrity of any part of the work, even ones in which the author was not personally involved, are appropriately investigated, resolved, and the resolution documented in the literature.

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Hans, F., Benning, L., Pooth, JS. et al. A potentially lifesaving error: unintentional high-dose adrenaline administration in anaphylaxis-induced cardiac arrest; a case report. Int J Emerg Med 17 , 78 (2024). https://doi.org/10.1186/s12245-024-00663-9

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Received : 15 February 2024

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DOI : https://doi.org/10.1186/s12245-024-00663-9

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